PubMed Commons is an experimental system of commenting on PubMed abstracts, introduced in October 2013. Comments are displayed on the abstract page, but during the initial closed pilot, only registered users can read or post comments. Any researcher who is listed as an author of an article indexed by PubMed is entitled to participate in the pilot. If you would like to participate and need an invitation, please email info@biomedcentral.com, giving the PubMed ID of an article on which you are an author. For more information, see the PubMed Commons FAQ.

I agree completely with this exciting article authors who state that MS, PD, and T2DM
are associated with endothelial dysfunction and carry an elevated risk for both micro
and macrovascular disease that are often present at the time of diagnosis of overt
T2DM. Postnatal vascularization in a response to injury mechanism to the endothelium
and the arterial vessel wall as well as the capillary bed result in most of the complications
associated with these disorders. I demonstrated, since 30 years, in early papers that
all individuals with Campbell de Morgan spots (cutaneous microangiomas) are involved
by a particular mitochondrial cytopathology, termed Congenital Acidosic Enzyme –Metabolic
Hystangiopathy-a (CAEMH-a) (1, 2, 3, 4), conditio sine qua non of diabetic, dyslipidemic,
arteriosclerotic, hypertensive, a.s.o., constitutions (See HONCode web site 233736,
www.semeioticabiofisica.it).

Really, we must consider the importance of bed side recognizing all these inherited
conditions, which play a paramount role in primary prevention of MS, PD, and T2DM,
among other common human diseases, including malignancy.

In fact, from the healthy stage, white zone, slowly, very slowly one can reach the
disease onset, black zone – DM, ATS, AI, dyslipidaemia, gout, malignancies,
a.s.o., going through the pre-morbid, pre-metabolic stage, or grey zone, that can
last years or decades, without any clinical symptomatology, which is the topic of
my comment, as far as arteriosclerosis (arterioscleropathy) and type 2 DM are concerned.

Metabolic syndrome, X syndrome, or Reaven’s syndrome, classic or “variant”,
I described years ago (5), represent the possible end of grey zone. Due to this reason,
we term the grew zone as pre-morbid or pre-metabolic syndrome (Oncological Terrain,
in above-cited site).

Interestingly, both grey zone and metabolic syndrome, classic or “variant”,
are based on Congenital Acidosic Enzyme-Metabolic Histangiopathy-a (CAEMH-a) (1,2,3,4
and the above-cited site), observable since birth-day obviously in individual CAEMH-a
positive. It is a functional mitochondrial cytopathology, inheredited, as a general
rule, from the mother, mainly asymptomatic in initial stages, as well as for long
time, before ending in poly-metabolic syndrome.

The main problem, we have to face and hopefully resolve, is, therefore, to recognize
and define “clinically” underlying molecular-biological events, characteristic
of grey zone by means of efficacious method, rapid to perform at the bed-side, as
Biophysical Semeiotics, meaning it as conceptual and operative tool.

In the method are implicit all future knowledges, and, thus, we ask this method –
but not only to logic-deductive method, according to our philosophy (4) to allow us
to recognize “clinically” pre-morbid syndrome, which represents the locus
of primary prevention of most severe human diseases (1-5). Therefore, as starting
point of our reasoning, it is to be found a biophysical semeiotic reading key, really
different from that, based on “classic” signs and symptoms, which are,
on the other hand, completely absent in pre-morbid stage or grey zone, which permits
us to correctly diagnose in a “quantitative” manner the pre-metabolic
syndrome, in easy and rapid way, during common physical examination, even performed
for whatever other reason.